In our HT rat model, network analysis revealed the possibility of EA acting through OPRM1 and related circRNAs together with negatively regulating the sympathetic adrenergic system through CRH and COMT. Meanwhile, during EA treatment vascular contraction and dilation function mediated by AGTR2 also synergized with neuroendocrine regulation, and negative regulation mainly functioned through GABAergic neurons. The gene discussed is CRH; the disease is hematocrit.